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Feature article summaries and commentary on a variety of VIR topics such as uterine fibroid and prostate embolization, angioplasty, chemoembolization, and endovascular treatment of peripheral arterial disease.

Peripheral artery disease (PAD), including femoropopliteal artery disease, has been proposed as a “coronary heart disease risk equivalent” in the National Cholesterol Education Program Adult Treatment Panel III. Patients with femoropopliteal arterial disease are strong candidates for statin therapy. The effect of statin therapy on femoropopliteal arterial disease has received relatively little attention in the literature. This manuscript evaluated 135 limbs in 135 patients in whom nitinol stents were placed in femoropopliteal occlusions and found that the incidence of binary restenosis was significantly lower in the statin group than in the nonstatin group.

Clinical Pearls

What are the TransAtlantic Inter-Society Concensus (TASC) II classifications of femoral popliteal lesions? The following diagram illustrates the TASC II classification of femoropoliteal disease as described by Norgren et al. in the Journal of Vascular Surgery in January of 2007.

This study aimed for goals of a residual pressure gradient of less than 10 mm Hg, residual stenosis of less than 30%, or no flow-limiting dissection after nitinol stent implantation according to TASC II. 91.1% of lesions treated in this study were TASC II type C or D.

What are the American College of Cardiology and American Heart Association guidelines for intensity of statin therapy?

The “2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults” established algorithms to decide initiation and dosing of statin therapy.

Morning Report Questions

What were the methods to follow-up patients after femoropopliteal revascularization with nitinol stenting?

The authors in this study evaluated patients for follow-up within 30 days of the index procedure, which included an assessment of the patient’s clinical improvement as well as interval ankle-brachial index (ABI) and duplex ultrasound (US) scanning. Follow-up was then conducted every 3–6 months during the first postoperative year and every 6–12 months thereafter. In cases of suspected restenosis based on the clinical evaluation and arterial noninvasive examination, lower-extremity computed tomographic angiography could be performed at the discretion of the operator. The primary endpoint of the study was binary restenosis (angiographic luminal narrowing > 50% in diameter anywhere within the stent or within the 5-mm proximal or distal border of the stent or peak systolic velocity ratio of > 2.54 by duplex US) at 1 year. Secondary endpoints were primary patency at 1 year, binary restenosis at 2 years, and target lesion revascularization (TLR; repeat revascularization of the target lesion secondary to restenosis of more than 50% within the stent or 5 mm proximal or distal to the stent) at 2 years

In the present study, a total of 135 limbs (91.1% TASC II type C or D lesions) of 135 patients were included in the analysis. 91 (67.4%) received statin therapy and 44 (32.6%) did not. Equivalent proportions of patients in each group were treated with aspirin, thienopyridine derivatives, and cilostazol. The total stent implanted length and mean stent diameter did not differ between groups. The mean follow-up duration was 16.9 months. There were significant differences in the incidence of binary restenosis between groups at 1 year (45.5% for the nonstatin group vs 28.6% for the statin group; P = .05) and 2 years. Primary patency rates at 1 year were 50.5% in the nonstatin group and 72.5% in the statin group (P = .01). The 2-year TLR rates were 54.5% in the nonstatin group and 35.2% in the statin group (P = .03). The odds of binary restenosis at 1 year were not affected after adjustment for age, sex, and other cardiovascular risk factors.

What is the mechanism of cilostazol and how might it have confounded the study?

Cilostazol is a phosphodiesterase (PDE) III inhibitor with vasodilator, metabolic, and antiplatelet activity. The TASC II analysis reported benefits of cilostazol over placebo in treadmill performance and quality of life measures with side effects of headache, diarrhea, and palpitations. Because it is a PDE III inhibitor, it should not be given to patients with congestive heart failure. Recent studies have demonstrated that that long-term cilostazol therapy was able to reduce restenosis after endovascular therapy in symptomatic patients with femoropopliteal artery disease. Although the use of cilostazol was statistically equivalent between the two groups in the present study, the rates of binary restenosis and TLR might be affected according to the proportion of patients receiving cilostazol therapy.

How may future studies be affected by increasing statin use?

Some patients in the nonstatin group of this study included those with hypertension, CAD, or a history of percutaneous coronary intervention. It is possible that these and other patients with transient ischemic attack or minimal coronary artery stenosis may have been followed up without the use of statins, even though that is not considered the standard of care. The Reduction of Atherothrombosis for Continued Health Registry showed that the rate of statin use at baseline was only 62.2% in patients with PAD, and one third of the nonstatin group had a history of CAD or cerebrovascular disease. They observed differences in statin use based on physician subspecialty or patient age. The use of statins has become more common, but a high prevalence of statin use among patients with PAD in the future will make it challenging to design clinical studies to evaluate the role of statin therapy as an inhibitor of restenosis after nitinol stent implantation in patients with femoropopliteal artery disease.